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Gene expression profiles in the ileal and colonic epithelial cells from Interleukin (IL)-23-deficient mice and IL-22-deficient mice

ABSTRACT: Gene expression profiles in the ileal and colonic epithelial cells from Interleukin (IL)-23-deficient mice and IL-22-deficient mice

PROVIDER: PRJNA990813 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25118826.fastq.gz	Fastqsanger.gz
	SRR25118827.fastq.gz	Fastqsanger.gz
	SRR25118828.fastq.gz	Fastqsanger.gz
	SRR25118829.fastq.gz	Fastqsanger.gz
	SRR25118830.fastq.gz	Fastqsanger.gz

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Gene expression profiles in the ileal and colonic epithelial cells from Interleukin (IL)-23-deficient mice and IL-22-deficient mice

Project description:To investigate the function of IL-23 and IL-22 on the intestinal epithelial cells, we analyzed the gene expression profiles in ileal and colonic epithelial cells of mice deficient in IL-23 and IL-22.

2023-09-08 | GSE236445 | GEO

Proteomic analysis of platelets isolated from mice deficient for IL-33 or treated with recombinant IL-33

Project description:Platelets, traditionally recognized for their involvement in hemostasis and wound healing, also play a central role in immune regulation and inflammation. Their function and production adapt in response to inflammatory cues such as cytokines and danger-associated molecular patterns. Interleukin-33 (IL-33), an alarmin released during tissue damage, particularly in lung inflammation, has been implicated in influencing platelet biology, though its exact effects remain poorly understood. To clarify IL-33’s role, we examined its impact on platelet proteome. We first compared the proteome of platelets purified by FACS from IL-33-deficient (IL-33KO) mice versus WT mice (n=5 biological replicates in each group, 10 raw MS files). We also compared the proteome of platelets from WT mice which were either non stimulated (n= 8 biological replicates) or treated intranasally with recombinant IL-33 (n= 9 biological replicates).

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Colonic transcriptomic data of interleukin-10-deficient mice

Project description:Inflammatory bowel disease (IBD) is a chronic relapsing autoimmune disease of gastrointestinal tract (GI), involving in dysfunction of a variety of genes, such as Interleukin (IL)-10. Intense researches have demonstrated that IL10-deficient (IL10-/-) mice gradually exhibits features of spontaneous enterocolitis at 4-8 weeks of age and IL-10 is a significant immunomodulator in intestinal tract. Therefore, IL10-/- mice have become a classic model of enterocolitis to study the pathogenesis of IBD. To uncover the role of the underlying molecular mechanisms involved in IL10-/--associated chronic colitis, we constructed IL10-deficient mice and sequenced transcriptome of colon tissues from the mice with colitis in this study. Mechanically, we might find out new therapeutic targets for IBD according to the omics analysis.

2025-05-01 | GSE264294 | GEO

Whole Lung Proteome in N. brasiliensis Infection in IL-13 deficient mice.

Project description:IL-13 plays a key role during protective type 2 immune responses at mucosal sites, such as during infection with nematodes. However, dysregulation of IL-13 can also contribute to the pathogenesis of allergic and fibrotic diseases. Matrix remodelling is an important component of repair processes in the lung but is also a hallmark of chronic diseases such as asthma. Since IL-13 shares receptors and signalling pathways with IL-4, disentangling the relative contributions of these two type 2 cytokines has been challenging. Additionally, little is known about the singular role of IL-13 in more acute settings of tissue injury/repair and whether IL-13 regulates remodelling of the extracellular matrix following tissue injury. In this study, we used Nippostrongylus brasiliensis infection as model of acute lung tissue damage and repair by comparing responses between WT and IL-13-deficient mice, in which IL-4 signalling is intact.

2021-06-11 | PXD021853 | Pride

Dysregulated neutrophil response drives lethality during Citrobacter rodentium infection in interleukin-22 deficient mice

Project description:Citrobacter rodentium (CR) is a murine enteric pathogen widely used to model attaching and effacing bacterial disease caused by enteropathogenic and enterohaemorrhagic Escherichia coli. Infection induces colonic epithelial damage and inflammation that resolves in resistant mice but results in severe disease and mortality in mice lacking interleukin-22 (IL-22). Although IL-22 promotes antimicrobial responses, epithelial barrier integrity and tissue repair during infection, the inflammatory mechanisms responsible for lethality in its absence remain poorly defined. Here, we tested whether dysregulated neutrophil responses drive disease progression in IL-22-deficient (Il22-/-) mice. Using a murine model of CR infection, we show that IL-22 deficiency is associated with progressive colonic pathology and the early emergence of a neutrophil-rich inflammatory state, characterised by markedly increased neutrophil recruitment, accumulation, and effector activity in the colonic mucosa. To determine whether excessive neutrophil responses are required for lethality, we exploited deletion of the CR type III secretion system effector EspO, a bacterial factor that promotes neutrophil recruitment. EspO deletion substantially reduced neutrophil accumulation and activity in Il22-/- mice without altering bacterial burden. Strikingly, infection with CR ΔEspO resulted in reduced colonic inflammation and 100 percent survival of infected Il22-/- mice. Together, these findings identify excessive neutrophil accumulation and activity as a key driver of lethality during CR infection in Il22-/- mice and suggest how a bacterial virulence factor amplifies neutrophil-dependent pathology within a vulnerable epithelial environment.

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Project description:The Th2 cytokine IL-13 has been described to be involved in biliary epithelial injury and liver fibrosis in patients as well as in animal models. IL-13 was found to reduce tight junction-associated barrier function of bile ducts, to promote cholangiocyte hyperplasia, and thus causing biliary epithelial injury. We generated Abcb4-/-- and IL-13-/- double-knockout mice on fibrosis susceptible genetic background BALB/c. Molecular and cellular mechanisms of hepatic and ileal pathology were investigated by mRNA microarray. Depletion of IL-13 in Abcb4-/--mice resulted in a tenfold decrease of total serum bile acid concentrations at the age of 8 weeks and lead to a recovery of intrahepatic bile duct integrity. The decrease of serum bile acid in 8 week old mice went along with relative enhancement of bile acid excretion and normalization of the composition of fecal bile excretion, correction of fecal microbiome, and improved ileal integrity. Liver integrity, measured by serum ALT, was ameliorated in younger mice and strongly correlated with the concentration of serum bile acids. 52 weeks old Abcb4-/-IL-13-/--mice exhibited significantly reduced hepatic fibrosis.

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Metformin Improves Ileal Epithelial Barrier Function in Interleukin-10 Deficient Mice.

Project description: Not available

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Analysis of Colonic and Ileal Samples from Axenic Mice.

Project description:This dataset provides a comprehensive lipidomics analysis of ileal and colonic content extracts from axenic mice, performed using high-resolution mass spectrometry in ESI negative mode.

2025-04-06 | MSV000097546 | MassIVE

Accelerated wound healing phenotype in Interleukin 12/23 deficient mice.

Project description: Not available

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Colonic transcriptomic and proteomic profiling provides new insight into the pathogenesis of chronic colitis in interleukin-10-deficient mice

Project description:Inflammatory bowel disease (IBD) is a chronic relapsing autoimmune disease of gastrointestinal tract (GI), involving in dysfunction of a variety of genes, such as Interleukin (IL)-10. Intense researches have demonstrated that IL10-deficient (IL10-/-) mice gradually exhibits features of spontaneous enterocolitis at 4-8 weeks of age and IL-10 is a significant immunomodulator in intestinal tract. Therefore, IL10-/- mice have become a classic model of enterocolitis to study the pathogenesis of IBD. The prevailing view is that IL10 deficiency leads to abnormal activation of immune cells and overproduction of a range of inflammation-inducing cytokines, which results in the persistence of intestinal inflammation in the mice. To uncover the role of the underlying molecular mechanisms involved in IL10-/--associated chronic enterocolitis, we construct IL10-deficient mice, sequence transcriptome and proteome of colon tissues from the mice with colitis and perform an integrated analysis of the two omics in this study. Mechanically, we might find out several novel signaling pathways or new therapeutic targets for IBD according to this combined analysis.

2024-04-26 | PXD051806 |

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